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. 2011 Jan;48(1):3-7.
doi: 10.3164/jcbn.11-007FR. Epub 2010 Dec 28.

Do free radicals play causal role in atherosclerosis? Low density lipoprotein oxidation and vitamin E revisited

Etsuo Niki  1
Affiliations

Do free radicals play causal role in atherosclerosis? Low density lipoprotein oxidation and vitamin E revisited

Etsuo Niki. J Clin Biochem Nutr. 2011 Jan.

Abstract

Lipid peroxidation induced by free radicals has been implicated in the pathogenesis of various diseases. Numerous in vitro and animal studies show that oxidative modification of low density lipoprotein (LDL) is an important initial event of atherosclerosis. Vitamin E and other antioxidants inhibit low density lipoprotein oxidation efficiently in vitro, however, human clinical trials with vitamin E have not yielded positive results. The mixed results for vitamin E effect may be ascribed primarily to the two factors. Firstly low density lipoprotein oxidation proceeds by multiple pathways mediated not only by free radicals but also by other non-radical oxidants and vitamin E is effective only against free radical mediated oxidation. Secondly, in contrast to animal experiments, vitamin E is given at the latter stage where oxidation is no more important. Free radicals must play causal role in pathogenesis of atherosclerosis and vitamin E should be effective if given at right time to right subjects.

Keywords: atherosclerosis; biomarker; free radical; lipid peroxidation; vitamin E.

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Figures

Fig. 1
Fig. 1
Progress of atherosclerosis and vitamin E supplementation (see text).
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References

    1. Steinberg D, Parthasarathy S, Carew TE, Khoo JC, Witztum JL. Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med. 1989;320:915–924. - PubMed
    1. Steinberg D. The LDL modification hypothesis of atherogenesis: an update. J Lipid Res. 2009;50(Suppl):S376–S381. - PMC - PubMed
    1. Miller YI, Choi SH, Fang L, Tsimikas S. Lipoprotein modification and macrophage uptake: role of pathologic cholesterol transport in atherogenesis. Subcell Biochem. 2010;51:229–251. - PubMed
    1. Shao B, Oda MN, Oram JF, Heinecke JW. Myeloperoxidase: an oxidative pathway for generating dysfunctional high-density lipoprotein. Chem Res Toxicol. 2010;23:447–454. - PMC - PubMed
    1. Berliner JA, Territo MC, Sevanian A, et al. Minimally modified low density lipoprotein stimulates monocyte endothelial interactions. J Clin Invest. 1990;85:1260–1266. - PMC - PubMed